Takase B, Akima T, Uehata A, Katushika S, Isojima K, Satomura K, Ohsuzu F, Kurita A
National Defense Medical College, Internal Medicine-1, Tokorozawa, Saitama, Japan.
Clin Cardiol. 2000 Nov;23(11):820-4. doi: 10.1002/clc.4960231131.
Paradoxical peripheral vasodilation is one of the suspected mechanisms of neurally mediated syncope. Parasympathetic stimulation following sympathetic activation during orthostatic stress mainly contributes to this vasodilation.
Since endothelial function modulates peripheral vascular tone, this study aimed to determine whether endothelial function and inappropriate peripheral vasomotion has a significant role in the pathogenesis of neurally mediated syncope.
To investigate whether endothelial function is augmented or whether abnormal peripheral vasomotion exits, flow-mediated dilation (FMD, endothelium-dependent vasodilation) and sublingual glyceryl trinitrate-induced dilation (0.3 mg, GTN-D, endothelium-independent vasodilation) were measured in the brachial artery in 16 patients with neurally mediated syncope, aged 33 +/- 10 years, by using high-resolution ultrasound. All patients underwent positive head-up tilt testing. These measures were compared with those in 16 control subjects matched with the patients by age, gender, and coronary risk factors. For FMD, percent diameter changes were obtained from baseline to hyperemic conditions (1 min after 5 min occlusion of the forearm artery). There were five smokers in both the patient and the control groups, but there was no structural heart disease in either group.
Baseline brachial artery diameters were comparable (3.8 +/- 0.6 vs. 3.8 +/- 0.7 mm, NS). Flow-mediated dilation in patients with neurally mediated syncope had a normal value of 9.8 +/- 5.0% despite the inclusion of five smokers. Flow-mediated dilation and GTN-D in patients with neurally mediated syncope were significantly greater than those in controls (9.0 +/- 5.0 vs. 3.0 +/- 3.5%, p<0.05; 18.4 +/- 5.5 vs. 14.1 +/- 4.4%, p<0.05).
Augmented endothelial function and/or abnormal peripheral vasomotion in peripheral arteries are important in patients with neurally mediated syncope in selected populations.
反常性外周血管扩张是神经介导性晕厥的疑似机制之一。直立应激期间交感神经激活后的副交感神经刺激是这种血管扩张的主要原因。
由于内皮功能调节外周血管张力,本研究旨在确定内皮功能和不适当的外周血管运动在神经介导性晕厥的发病机制中是否起重要作用。
为了研究内皮功能是否增强或是否存在异常的外周血管运动,对16例年龄为33±10岁的神经介导性晕厥患者,使用高分辨率超声测量其肱动脉的血流介导的血管舒张(FMD,内皮依赖性血管舒张)和舌下硝酸甘油诱导的血管舒张(0.3mg,GTN-D,非内皮依赖性血管舒张)。所有患者均进行了阳性直立倾斜试验。将这些测量结果与16名在年龄、性别和冠心病危险因素方面与患者匹配的对照受试者的测量结果进行比较。对于FMD,从前臂动脉闭塞5分钟后1分钟的充血状态到基线状态获取直径变化百分比。患者组和对照组各有5名吸烟者,但两组均无结构性心脏病。
肱动脉基线直径相当(3.8±0.6对3.8±0.7mm,无显著性差异)。尽管纳入了5名吸烟者,但神经介导性晕厥患者的血流介导的血管舒张正常值为9.8±5.0%。神经介导性晕厥患者的血流介导的血管舒张和GTN-D显著大于对照组(9.0±5.0对3.0±3.5%,p<0.05;18.4±5.5对14.1±4.4%,p<0.05)。
在特定人群的神经介导性晕厥患者中,外周动脉内皮功能增强和/或外周血管运动异常很重要。